The β-blocker carvedilol and the benznidazole modulate the cardiac immune response in the acute infection induced by Colombian strain of the Trypanosoma cruzi

BACKGROUND The infection led by Trypanosoma cruzi persists in mammalian tissues causing an inflammatory imbalance. Carvedilol (Cv), a non-selective beta blocker drug indicated to treat heart failure and antihypertensive has shown to promote antioxidant and immunomodulatory properties which might imp...

Full description

Saved in:
Bibliographic Details
Published in:Memórias do Instituto Oswaldo Cruz Vol. 113; no. 11; p. e180271
Main Authors: Horta, Aline Luciano, Figueiredo, Vivian Paulino, Leite, Ana Luisa Junqueira, Costa, Guilherme de Paula, Menezes, Ana Paula de Jesus, Ramos, Camila de Oliveira, Pedrosa, Tamiles Caroline Fernandes, Bezerra, Frank Silva, Vieira, Paula Melo de Abreu, Talvani, André
Format: Journal Article
Language:English
Published: Brazil Instituto Oswaldo Cruz, Ministério da Saúde 18-10-2018
Fundação Oswaldo Cruz (FIOCRUZ)
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:BACKGROUND The infection led by Trypanosoma cruzi persists in mammalian tissues causing an inflammatory imbalance. Carvedilol (Cv), a non-selective beta blocker drug indicated to treat heart failure and antihypertensive has shown to promote antioxidant and immunomodulatory properties which might improve the inflammation induced by T. cruzi. OBJECTIVES Evaluate the role of Cv on the inflammatory response of C57BL/6 mice acutely infected with the Colombian strain of T. cruzi. METHODS Animals were infected with the Colombian strain of T. cruzi and treated with Cv (25 mg/kg/day), benznidazole (Bz) (100 mg/kg/day) or their combination. On the 28th day of infection and 23 days of treatment, the euthanasia occurred, and the heart preserved for histopathological, oxidative stress (SOD, catalase, TBARs, carbonylated proteins) and plasma (CCL2, CCL5, TNF, IL-10) analyses. Parasitaemia and survival were assessed along the infection. FINDINGS Cv decreased TBARs, but increased the mortality rate, the parasitaemia and the levels of CCL2, CCL5, catalase and the inflammatory infiltrate in the cardiac tissue. Bz led the reduction of the inflammatory infiltrate and circulating levels of oxidative stress and inflammatory mediators in the infected mice. MAIN CONCLUSIONS Our data suggest that Cv, in this experimental model using the Colombian strain of T. cruzi, caused damage to the host.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
AT, GPC and ALH - Scientific/financial conception of the study; ALH, VPF, ALJL, GPC, APJM and TCFP - parasitological, therapeutically and immunological data collection and analysis; FSB and COR - oxidative stress experiments and analysis; PMAV - pathological analysis; AT and ALH - data interpretation and drafting of the article.
ISSN:0074-0276
1678-8060
1678-8060
DOI:10.1590/0074-02760180271